Regular ArticleExpression Pattern of the Rett Syndrome Gene MeCP2 in Primate Prefrontal Cortex
References (28)
- et al.
Methylation-induced repression—Belts, braces, and chromatin
Cell
(1999) - et al.
Rett syndrome: Criteria for inclusion and exclusion
Brain Dev.
(1985) - et al.
DNA methyltransferases DNMT3a and DNMT3b are essential for de novo methylation and mammalian development
Cell
(1999) - et al.
Higher concentrations of macroH2a in the Barr body are correlated with higher nucleosome density
Curr. Biol.
(2000) - et al.
Rett syndrome and beyond: Recurrent spontaneous and familial MeCP2 mutations at CpG hotspots
Am. J. Hum. Genet.
(1999) Rett syndrome: Neurobiological changes underlying specific symptoms
Prog. Neurobiol.
(1997)- et al.
Characterisation of transcriptionally active and inactive chromatin domains in neurons
J. Cell Sci.
(2000) Diagnostic and Statistical Manual of Mental Disorders
(1994)- et al.
Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2
Nature Genet.
(1999) The neuropathology of the Rett syndrome
Brain Dev.
(1992)
Pervasive neuroanatomic abnormalities of the brain in three cases of Rett's syndrome
Neurology
Monoclonal antibody to neurofilament protein (SMI-32) labels pyramidal neurons in the human and monkey neocortex
J. Comp. Neurol.
Deficiency of methyl-CpG binding protein-2 in CNS neurons results in a Rett-like phenotype in mice
Nature Genet.
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2016, Schizophrenia ResearchCitation Excerpt :To further confirm the neuronal phenotype of NeuN immunoreactive white matter nuclei, we performed NeuN immunohistochemistry/DAPI counterstain on immersion-fixed, paraffin-embedded tissue blocks from the ventrolateral PFC of N = 3 clozapine-treated animals with elevated white matter neuron densities. Remarkably, when examining white matter NeuN+ nuclei under the microscope, 150/150 nuclei counted bear hallmarks characteristic for neuronal nuclei, including a prominent nucleolus with heterochromatic shell (Akbarian et al., 2001; Akhmanova et al., 2000; Thatcher and LaSalle, 2006) and/or a decondensed chromatin with overall much less compacted (hetero-)chromatin as compared to the surrounding non-neuronal (NeuN−) nuclei (subset of 3 monkeys, 50 white matter nuclei counted per monkey with a minimum diameter of 8 μm, see Supplemental Fig. 3). Next, we examined whether the molecular ‘fingerprint’ of NeuN+ nuclei is altered after clozapine exposure, by measuring the expression of RBFOX3 encoding the neuron-specific NeuN protein, and ABCA2 (ATP Binding Cassette 2), a gene predominantly expressed by white matter oligodendrocytes (Zhou et al., 2001).
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